What is it about?
Diabetes is associated with impaired wound healing, which may be caused primarily by a deficiency in dendritic epidermal T cells (DETCs). In the epidermis, IL-15, IGF-1, and mTOR are known to regulate the maintenance of DETCs; however, it is unclear how these molecules may intersect to regulate DETC homeostasis in diabetes. Here, we show that the reduction of DETCs in the epidermis of diabetic mice is caused by altered homeostasis mediated by a reduction in IL-15 levels. Both impaired mTOR activation and reduction of IL-15 in the epidermis play important roles in DETC homeostasis.
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Why is it important?
we revealed the intersecting roles of IGF-1, mTOR and IL-15 in regulating the reduced homeostasis of DETCs in a diabetic mouse model. We further defined a signaling network that, when impaired in diabetes, leads to decreased DETC homeostasis. These findings provide an increased understanding of factors regulating wound healing in diabetic mice, which could help to develop therapies for diabetic patients.
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This page is a summary of: Weakened IL-15 Production and Impaired mTOR Activation Alter Dendritic Epidermal T Cell Homeostasis in Diabetic Mice, Scientific Reports, July 2017, Nature,
DOI: 10.1038/s41598-017-05950-5.
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